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Peters Lectures Flashcards

1
Q

How is specificty of signalling achieved in the endocrine system?

A
  • chemically distinct hormones
  • specific receptors for each hormone
  • distinct distribution of receptors across target cells
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2
Q

What is the difference between the glands in the endocrine and exocrine systems?

A

endocrine glands are ductless

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3
Q

What are the 4 chemical types of homrone?

A

modified amino acids; steroids; peptides; proteins

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4
Q

What are the features of hormone control?

A

act a low concentration over large distances to activate specific receptors with high potency to integrate organ function

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5
Q

How is hormone action terminated?

A

by enzyme-mediated metabolic inactivation in the liver or at sites of action

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6
Q

How are amine hormones stored and released?

A

pre-synthesised, stored in vesicles. when ligand binds to cell receptor, calcium enters the cell and mediates exocytosis

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7
Q

How are peptide and protein hormones stored and released?

A

pre-synthesised usually from a longer precursor, stored in vesicles, released in response to stimuli by calcium-deoendent exocytosis

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8
Q

What enzymes convert the precursor protein to the mature hormone?

A

convertases during intracellular transport

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9
Q

What is the difference between steroid synthesis and release compared to that of amines and proteins?

A

steroids are synthesised and secreted upon demand, are not presynthesised and stored in vesicles

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10
Q

What effect does stimuli have on the synthesis of steroids?

A

stimuli increase:

  • cellular uptake and availability of cholesterol
  • rate of conversion of cholesterol to pregnenolone (rate limiting step)
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11
Q

What are the functions of carrier proteins?

A

to increase amount of hormone tranported in the blood; provise a reservoir of hormone and extend the half-life of the hormone in the circulation

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12
Q

What are two important general carrier proteins?

A

albumin; transthyretin

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13
Q

Why does free concentration of hormone not rise abruptly?

A

surges in hormone secretion are buffered by biding to carriers-they mop up the extra hormone

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14
Q

What type of hormone can corss the capillary wall to activate receptors in target tissues?

A

free hormone

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15
Q

What is the main determinant of plasma concentration?

A

rate of secretion

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16
Q

What factors contraol secretion?

A

negative feedback; neuroendocrine (eg stress); diurnal rhythm (rate fluctuates as a function of time)

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17
Q

What does tropic mean in relation to hormones?

A

a hromone that acts upon a nother endocrine gland to resulgate its secretion of hormone

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18
Q

Aside from secretion, what other factor contributes to plasma concentration?

A

rate of elimination

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19
Q

What are the 3 types of hormone receptor?

A

GPCR; receptor kinases; nuclear receptors

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20
Q

What are the classes of nuclear receptor?

A

class 1; class 2 and hybrid class

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21
Q

What hormone activates class 1?

A

steroid hormones

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22
Q

What do class 1 recetpros do in absence and presence of activating ligand?

A

in absence- located in the cytoplasm bound to inhibitor heat shock proteins, when activated, move to the nucleus

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23
Q

What type of hormone activates class 2 nuclear receptors?

A

lipids

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24
Q

Where are class 2 receptors found?

A

in the nucleus

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25
What hormones act of hybrid class of receptors?
thyroid hormones
26
What other class of receptor is hybrid class similar to?
class 1
27
What enzyme converts ATP to cAMP?
adenylyl cyclase
28
What does cAMP do?
increases the amoutn of protein kinase A which phosphorylates target proteins
29
What type of G protein increases action of adenylyl cyclase?
Gs
30
What type of G protein inhibits adenylyl cyclase?
Gi
31
What enxyme does Gq receptors increase the activity of?
phospholipase C
32
What two molecules does phosphlipase C create from PIP2?
IP3 and DAG
33
What is the action of DAG?
activates protein kinase C which phosphorylates target proteins
34
What does IP3 do?
works on IP3 receptors on the endoplasmic reticulum(or sarcoplasmic reticulum in muscle cells) to `release calcium
35
Give an exmple of a hormone which signals via receptor kinases?
insulin
36
What does binding of a ligand to a receptor kinase cause?
autophosphorylation of intracellular tyrosine residues
37
What proteins do the phosphorylated tyrosines then phosphorylate?
insulin receptor substrate proteins
38
What happens to the class 1 nuclear recetor when it moves into the nucleus (when activated and bound to steroid)?
forms a dimer and binds to hormone response elements in DNA
39
What does the binding of the dimer to hormone receptor elements inthe DNA cause?
transcrition of specific genes to tbe switched on (transactivated) or switched off (transrepressed)
40
What are the 4 methods of action of drugs for T2DM?
increasing secretion of insulin; decreasing insulin resistane and reducing hepatic glucose output; slowing glucose absorption from the GI tract; enhancing glucose excretion by the kidney
41
What drugs at by increasing secretion of insulin?
SUs; incretin mimicsl glinides; gliptins
42
What causes the Katp channel to open?
ADP-Mg binding to the SUR1 subunit
43
Give examples of sulfonyureas?
tolbutamide; glibenclamide; glipizide
44
What is the action of SUs?
displace the binding of ADP-Mg from the SUR1 subunit
45
What are the side effects of SUs?
hypoglyaemia; weight gain
46
How do glinides work?
bind to SUR1 to close the Katp channel
47
Why are glinides less likely to cause hypoglycaemia than SUs?
have rapid osnet/offset kinetics
48
What are the actions of GLP-1?
enhance insulin release; delay gastric emptying; decrease glucagon release
49
Give an example of an incretin analogue?
extenatide
50
How does extenatide work?
binds to GPCR GLP-1 receptors that increase intracellular cAMP conc.
51
What are actions of extenatide?
increases insulin secretion; suppresses glucagon secetion; slows gastric emptying and decreases appetite
52
How is extenatide administered?
subcutaneously
53
What are the side effects of extenatide?
nausea; hypo; pancreatitis
54
What does the enzyme dipeptidyl peptidase-4 do?
temrinates the actions of GLP-1 and GIP
55
What is the mode of action of gliptins?
competitively inhibit DPP-4, prolonging the actions of GLP-1 and GIP
56
What is alpha-glucosidase?
a brush border enzyme that breaks down starch and disaccharides to absorbale glucose
57
What are the side effects of alpha-glucosidase inhibitors?
flatulence; loose stools; diarrhoea; abdominal pain; bloating
58
What are the actions of metformin?
reduces hepatic gluconeogensis; increases glucose uptake; reduces carbohydrate absorption; increases fatty acid oxidation
59
What are the good things about metformin?
doesnt cause hypos; causes weight loss
60
What are the side effects of metformin?
GI upset; lactic acidosis
61
What is the mode of action of TZDs?
enhance the action of insulin at target tissues by acting on the PPARy nuclear receptor
62
What are benefits of TZDs?
promote FA uptake and storage in adipocytes rather than in SK and liver; reduces hetpatic glucose output
63
What are the adverse effects of TZDs?
weight gain; fluid retention; increased incidence of bone fractures
64
What is the action of SGLT inhibitors?
act to selectively block the reabsorption of glucose by SGLT2 in the proximal tubule of the kidney tubule

Endocrine (27 decks)

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